Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042109 (urticaria)
 6,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human keratinocytes are able to synthesize and express cell surface moieties characteristic of effector and/or accessory cells of the immune system (CD16, CD36, HLA-DR, intercellular adhesion molecule-1). In the present study, skin biopsies from healthy volunteers, from patients with psoriasis vulgaris (PV), mycosis fungoides (MF), purpura pigmentosa chronica (PPC), acute urticaria (AU) and from positive tuberculin skin tests were investigated with regard to the reactivity with the monoclonal antibodies to complement receptors CR1 CR2 and CR3 by means of a multistep immunoperoxidase method. In the clinically involved skin of all patients with PV, MF or PPC, and in biopsies obtained from positive tuberculin tests, specific epidermal intercellular staining with OKB7 and Leu anti-CR2 was seen on subcorneal keratinocytes. This finding suggests a differentiation-linked expression of CR2 on human keratinocytes in cytokine-mediated skin diseases whereas CR1 and CR3 are apparently not expressed.
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PMID:Expression of complement receptor CR2 (CD21) on human subcorneal keratinocytes in normal and diseased skin. 183 41

We have investigated the kinetics of the leucocyte infiltrate in delayed pressure urticaria (DPU) in relation to the in vivo expression of the cytokine-regulated cell surface adhesion molecules, E-selectin (endothelial adhesion molecule-1, ELAM-1), intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1). Immunohistochemical analysis was performed on biopsies taken from unchallenged skin, and at 0, 2, 6, 24, 48 and 120 h after weighted rods had been applied to 13 patients with DPU. There was moderate to marked upregulation of E-selectin at 6 and 24 h after application of pressure. At 24 h, more patients showed expression of VCAM-1 on perivascular cells than before pressure. Moderate expression of ICAM-1 was present in some biopsies from both unchallenged and pressure-challenged skin, but there was no clear trend. In DPU, there was a significant increase in the neutrophil count at 2 h after a pressure challenge, with further increases at 6 and 24 h. The median cell counts per high-power field of eosinophils and monocyte/macrophages increased significantly at 24 h after pressure. Biopsies from four normal controls subjected to an identical pressure challenge showed no detectable changes in adhesion molecule expression or in the cell infiltrate. The findings in four patients with chronic idiopathic urticaria not associated with DPU were qualitatively similar to (but intermediate in severity between) the findings in DPU weals at 6 and 24 h. These results suggest that vascular endothelial activation is an early response to pressure challenge in DPU, and is also present in chronic idiopathic urticaria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adhesion molecule expression and the inflammatory cell infiltrate in delayed pressure urticaria. 752 16

Six patients with delayed pressure urticaria (DPU) applied clobetasol propionate (0.05%) ointment or its base to predetermined test sites on the right and left thigh as part of a randomized, double-blind study. A pressure challenge was administered to each test site at the initial visit and repeated after 3 days and 6 weeks of treatment and at between 4 and 8 weeks after treatment. The areas of pressure-induced weals were measured 6 h after each challenge. At the 6-week visit, a 4-mm punch biopsy was taken from pressure-challenged skin on each test site. Sections were stained for mast cells and immunohistochemical labelling was used to demonstrate neutrophils (neutrophil elastase), eosinophils (eosinophil cationic protein), monocytes/macrophages (EBM 11), cells expressing the beta-2 integrins (CD11/18) and the vascular adhesion molecules, E selectin and intercellular adhesion molecule-1 (ICAM-1). In the steroid-treated sites, there was a significant decrease (P < 0.05, Wilcoxon's matched-pairs test) in the size of the pressure weals compared with baseline at 3 days, 6 weeks and at follow-up. Demonstrable mast cells were significantly decreased (P = 0.059) in the pressure-challenged areas in the steroid-treated sites compared with the base-treated sites. The histological response to pressure was minimal in both sites perhaps demonstrating an active pharmacological effect of the ointment base. In conclusion, the application of potent topical steroids significantly reduced the clinical response to pressure in patients with DPU, possibly through a reduction in mast cells.
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PMID:The effects of topical corticosteroids on delayed pressure urticaria. 754 Nov 90

The results of several investigations proved that, in special circumstances, human keratinocytes (HKs) synthesize and express cell surface moieties characteristic of effector and/or accessory cells of the immune system, such as CD16, CD36, HLA-DR, and intercellular adhesion molecule-1 (CD54), which are all detectable on the surfaces of macrophages. In the present study, skin biopsies from healthy volunteers, from positive tuberculin skin tests, and from patients with acute urticaria (AU), lichen planus (LP), psoriasis vulgaris (PV), mycosis fungoides (MF), and purpura pigmentosa chronica (PPC) were investigated by means of a multistep immunoperoxidase method to examine the reactivity of the HKs with a panel of monoclonal antibodies (MABs) characteristic of monocyte/macrophage cell lines. In biopsies obtained from positive tuberculin tests and from clinically involved skin of patients with LP, PV, MF, or PPC, a multifocal, positive peroxidase reaction was observed on the membranes of HKs of the basal and suprabasal cell layers when the MABs OKM13 (CD13), OKM14 (CD14), and Dako-Macrophage (CD68) were used. In contrast, specific staining of the HKs was not observed with the same antibodies in the biopsies of healthy volunteers or of patients with AU or in the uninvolved skin specimens obtained from the other patients. The HKs of PV, LP, MF, PPC, and AU patients and those of the healthy subjects all failed to give positive reactions when MABs against CD11b, CD15, or CD33 were used. The published data supplement the known surface characteristics of HKs, reflecting their stage of activation and differentiation.
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PMID:Expression of monocyte/macrophage markers (CD13, CD14, CD68) on human keratinocytes in healthy and diseased skin. 768 77

The role of adhesion molecules; the intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) as mediators in development of skin allergy caused by giardiasis and the controlling role of the cytokine interleukin (IL)-6 over these adhesion molecules were studied. The work included 25 symptomatic giardiasis patients with skin allergy manifested by diffuse urticaria, pruritus, wheal and erythema, and had positive serum anti-Giardia immunoglobulin (Ig) E measured as mean optical density (OD) value by enzyme linked immunosorbent assay (ELISA), employed as an evidence of allergic sensitization (G.I). They were compared with 30 symptomatic giardiasis patients (G.II) and 20 apparently healthy control subjects (G.III), both latter groups had negative serum anti-Giardia IgE. The mean OD value of anti-Giardia IgE was significantly increased in G.I (P < 0.01) & insignificantly different in GIII (P > 0.05) compared with G.III. Serum levels of soluble forms of adhesion molecules; sICAM-1 & sVCAM-1, and IL-6 were determined by ELISA. sICAM-1 & sVCAM-1 serum levels were significantly increased (P < 0.001) in G.I compared with G.III and showed insignificant difference (P > 0.05) between Gs. II & III. Serum IL-6 significantly increased in G.I (P < 0.001) & G.II (P < 0.05) compared with G.III, and was significantly higher (P < 0.001) in G.I than G.II. Serum IL-6 correlated positively with serum sICAM-1 (P < 0.01) and sVCAM-1 (P < 0.001) in G.I. The results are discussed.
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PMID:Human giardiasis as an etiology of skin allergy: the role of adhesion molecules and interleukin-6. 1558 2